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Conclusion: When exercising in a hot-dry environment, airflow is required for rehydration to improve thermoregulation and cardiovascular function.

When exercising in a hot environment, evaporation is the most important heat-loss avenue (20). However, heat loss by evaporation is limited by the capacity of the environment to accept water vapor (i.e., inversely related to the humidity). Recognizing the importance of humidity, the American College Sports Medicine position stand on the prevention of thermal injuries during distance running (2) includes wet-bulb temperature as a factor to gauge the risk to develop heat injury when exercising in the heat. However, it is less well recognized that not only the humidity but also the velocity of the air moving around the body plays an important role in convective and evaporative heat loss.

When exercising in a 35°C environment, airflow (3 m·s−1) prevents esophageal temperature from increasing beyond 38°C after 60 min of moderate-intensity exercise (1). Paradoxically, the authors observed an increased whole body sweat rate in the still-air condition. However, without wind more of that sweat was not evaporated (inefficient sweating) and truly evaporative water loss was reduced at a given core temperature. Airflow restriction during cycling at a moderate intensity not only raises core temperature (23) but also heart rate, drift that is prevented in the presence of airflow (1,25). The observation that without wind skin blood flow and heart rate both increase (25) supports the theory that cardiovascular drift is originated by a redistribution of blood to the cutaneous circulation (22). However, to our knowledge the effects of airflow on skin blood flow and its relationship with the cardiovascular responses have not yet been investigated during exercise in a hot environment.

During exercise (60% V˙O2max) in the heat (33°C; 50% relative humidity) with airflow (2.5 m·s−1) a positive relationship has been reported between body water deficit (i.e., dehydration) and the increases in core temperature (11,18). However, this relationship has been recently disputed. Saunders et al., (23) found under similar experimental conditions (hot environment, moderate intensity exercise in trained subjects) that an increase in fluid intake did not reduce final core temperature. In that study airflow was delivered at a high velocity (9.3 m·s−1 = 33 km·h−1), which may have overridden the effects of the small increase in rehydration (from 60 to 80% of sweat losses). However, it is unclear whether airflow at velocities commonly encountered during running activities (from 5, up to 20 km·h−1) could override the thermoregulatory and cardiovascular benefits of rehydration during exercise in a hot environment.

During prolonged exercise in the heat, rehydration reduces hyperthermia by maintaining convective (skin blood flow) and evaporative heat loss (24). In contrast, hypohydration delays (14) and reduces (13) the skin blood flow and sweat response for a given level of core temperature. Thus, in a heat-compensable environment (capacity for evaporative heat loss exceeds heat production), rehydration is a key factor to prevent hyperthermia if airflow is allowed. However, in an uncompensable environment (limited evaporative heat loss) rehydration does not alter the rate of heat storage (16). One way to limit evaporative heat loss is to restrict air circulating over the skin. It is not uncommon that indoors exercise facilities lack proper ventilation. To the extent of our knowledge it is not known if the lack of airflow negates the effects of rehydration when fit, heat-acclimated subjects (i.e., with large potential for heat dissipation) exercise in a hot-dry environment. On the other hand, it is also unknown whether airflow alone is superior to rehydration on preventing hyperthermia during prolonged exercise in the heat.

The aim of this study was to investigate the separate and combined effects of airflow and oral rehydration on heat accumulation and dissipation during prolonged exercise in a hot-dry environment. We hypothesized that in a hot-dry environment, rehydration alone would not prevent the increases core temperature. A secondary aim was to investigate the effects of these treatments on the cardiovascular response to exercise in the heat.

METHODS

Subjects.

Ten moderately trained healthy men participated in the study. Subjects routinely trained for about 30 min·d−1, 2-3 d·wk−1 during the last year. They had a mean (± SD) age of 26 ± 5 yr, body mass of 74 ± 7 kg, height of 180 ± 5 cm, and maximal oxygen consumption (V˙O2max) of 55 ± 8 mL·kg−1·min−1. Written informed consent was obtained from each participant, and the local institutional ethics committee approved the study. A previous physical examination (including ECG) ensured that each participant was in good health.

Preliminary testing.

O2 consumption was collected every 15 s during an incremental cycling test to volitional fatigue. V˙O2max was measured as the highest plateau (two successive maximal readings within 0.15 L·min−1) reached. Each subject underwent seven consecutive days of heat acclimatization consisting of 1-h cycling bouts (60% V˙O2max) in a warm environment (35 ± 0.1°C and 27 ± 3% relative humidity without airflow). The rationale behind the acclimatization was to maximize the thermoregulatory adaptations before the onset of the experimental trials to avoid the bias of having subjects in progressive stages of heat acclimation.

Experimental design.

Experiments were conducted at the same time of the day for each subject (mostly in the afternoon) to avoid a circadian variation in internal body temperature. For the experimental trials subjects dressed in cycling shorts and cleated shoes. Subjects pedaled a cycle ergometer (900BP, Ergoline, Germany) continuously for 60 min in a hot-dry environment (36.3 ± 0.4°C; 29 ± 2% relative humidity) at a constant work rate that elicited 60% of their individual V˙O2max. Subjects performed four experimental trials in a randomized order separated by at least 48 h (but no more than 4 d, to avoid losing heat acclimation). Trials consisted of pedaling 1) without rehydration or forced airflow (control trial; CON); 2) rehydrating approximately 100% of sweat losses by ingesting a commercially available (i.e., Gatorade, Quaker Oats Co.) 6% carbohydrate-electrolyte solution (rehydration trial; REH); 3) receiving airflow at a wind velocity of 2.55 m·s−1 (wind trial; WIND); and 4) combining airflow and rehydration (wind plus rehydration trial; W + R). Environmental temperatures were recorded with a heat-stress monitor (WBGT, Wibget IST). Airflow at 2.55 m·s−1 was delivered towards the subject's chest by an industrial fan (50-cm blade diameter, V101, Photon, Spain), which was calibrated before the study using an anemometer (LCA30 VT, Airflow Ins). During REH and W + R, subjects were rehydrated with a carbohydrate-electrolyte solution because it has been shown to induce similar thermoregulatory and cardiovascular benefits than water ingestion, at least during exercise in the heat lasting about 60 min (3).

Fluid balance.

Subjects were instructed to ingest 500 mL of water 2 h before arriving to the laboratory to increase the likelihood they would begin the test in a euhydrated state. On arrival to the laboratory, a urine sample was collected in a sterilized container, and its specific gravity was immediately determined (Atago optical refreactometer, NSG Inc.). The volume of fluid ingested during the rehydration trials was calculated to replace 100% of the sweat losses (based on the sweat rate from the last acclimation bout). One third of the total volume (i.e., 1540 ± 136 mL) was ingested right before the start of the exercise, and the remaining volume in two aliquots after 15 and 30 min of exercise. To prevent body cooling from fluid ingestion, drinks remained inside the hot chamber for 45 min, and their average temperature at ingestion was 31°C. Whole-body sweat rate was calculated by subtracting pre- from postexercise nude body weight using a ± 0.05-kg-sensitive scale (WildCat; Metler, Toledo, OH), correcting for fluid intake, and exhalation of metabolic carbon and respiratory water (17).

Thermoregulatory responses.

Four superficial skin thermistors (408, YSI) were placed on the leg, thigh, chest, and arm, which allowed us to calculate mean skin temperature (TSK = 0.3(TCHEST + TARM) + 0.2(TTHIGH + TLEG); (21)). Rectal temperature (TREC) was measured by means of a flexible thermistor (401, YSI) positioned 15 cm past the anal sphincter. All thermistors were calibrated before the study using a water bath (Vertex, Velp, IT) and a reference high-resolution (0.1°C) mercury in-glass thermometer traceable to the German Bureau of Standards (Select, Proton, Spain). Forearm skin blood flow (SKBF) was measured using a laser Doppler flowmeter (Moor Lab, Moor Instruments, UK) positioned at the dorsum of the left forearm while the arm was supported by a sling at heart level. SKBF was normalized using each subject's preexercise value for that trial. All these probes were connected to a multichannel A/D board (PowerLab 8SP, ADI, UK) and associated software that displayed and stored data for 60 s every 10 min throughout the trials. Mean body temperature (Tbody) was calculated from rectal and skin temperature using weighting factors for exercise in a hot environment (Tbody = 0.79(TREC) + 0.21(TSK); (7)). Heatstorage (HS) was calculated from the increase in Tbodyduring exercise, preexercise body weight (BW) and surfacearea (AD = 0.202BW0.425 × height0.725; (10)) according to the equation proposed by Adams et al. (HS = 0.965BWTbody/AD; (1)). Potential heat loss by means of radiation, convection and evaporation were calculated following the equations proposed by Nielsen (20). Heat data are expressed in watts per square meter of body surface area per hour.

Blood analysis.

Thirty minutes before exercise, a Teflon catheter was inserted in the antecubital vein of the right arm. Blood samples (2 mL) were taken after 15 min of seated rest in the cycle ergometer and after 15 and 60 min of exercise. Blood was immediately analyzed for hemoglobin concentration (ABL-520; Radiometer, Denmark), and hematocrit was measured in triplicate by microcentrifugation and corrected for trapped plasma and venous sampling. Relative changes in blood volume and plasma volume were calculated with the equations outlined by Dill and Costill (9).

Thermoregulatory responses.

V˙O2 was similar during all trials and tended to increase with time of exercise. Thus, Mnet also tended to increase with exercise time (376 ± 16 to 388 ± 17 W·m−2·h−1; NS). Preexercise rectal temperatures (TREC; Fig. 1) were not different in any of the experimental conditions (mean across trials of 37.6 ± 0.1°C). TREC rose at a faster rate in CON and REH, being significantly higher than W + R at 60 min of exercise (P < 0.05). Without wind, fluid ingestion (REH) did not reduce rectal temperature below CON. However, with wind (2.55 m·s−1) fluid ingestion (W + R) reduced final TREC below WIND (P < 0.05). Mean skin temperature (TSK) was not significantly different at rest among trials. TSK during WIND and W + R tended to decline during exercise being both lower than CON after 60 min of exercise (Fig. 2A; P < 0.05). Forearm skin blood flow response (% from rest) to the treatments mimicked the TSK response with initial elevations and lower final values for the trials where wind was allowed (249 ± 46 and 225 ± 30% for WIND and W + R, and 263 ± 33, and 275 ± 27% for CON and REH, respectively). However, these differences did not reach statistical significance (Fig. 2B).

Cardiovascular responses.

Heart rate (HR) at rest was similar in all trials (68 ± 3 bpm). Already after 15 min of exercise, HR was lower during WIND than during REH and during W + R than during REH and CON (Table 2; P < 0.05). From 15 to 55 min of exercise, HR increased significantly only during the trials without wind (CON and REH). Cardiac output (Q˙) was similar in all trials after 15 min of exercise. However, in the trials with rehydration (REH and W + R), Q˙ was better maintained, being higher than CON after 55 min of exercise (Table 2; P < 0.05). Stroke volume (SV) responded opposite to HR being higher than CON and REH after 55 min of exercise in the trials with wind (WIND and W + R; P < 0.05). Furthermore, stroke volume at 55 min during W + R was higher than during WIND alone (P < 0.05). Mean arterial pressure was not different among trials and was well maintained during exercise despite dehydration (CON and WIND).

DISCUSSION

The novel finding of this study is that thermoregulatory benefits of rehydration during exercise in hot conditions depend on airflow. Full rehydration (93 ± 2% of sweat loss replaced; REH) did not reduce rectal temperature (TREC) below CON despite a 2% difference in dehydration (Fig. 1). Furthermore, REH did not increase whole body sweat rate or forearm skin blood flow in comparison with CON, both of which are mechanisms to increase heat dissipation. This was so despite using moderately trained, heat-acclimated subjects with a high heat-dissipation capacity and, thus, large potential to benefit from fluid ingestion.

Montain and Coyle (18) have observed that under similar conditions but with airflow (2.5 m·s−1), the differences in TREC between large rehydration (similar to our REH) and no fluid (similar to our CON) did not emerge until 80 min into exercise. It could then be argued that 60 min of exercise (present study) is not sufficient time to attain a dehydration level that would impair heat dissipation during CON and thus to observe a positive effect of fluid ingestion during REH. However, because of our higher sweat rate (1.65 vs 1.35 L·h−1) after 60 min, our subjects were dehydrated similarly to Montain and Coyle's data after 80 min (calculated assuming constant sweat rate). In addition, after 60 min of exercise in CON, TREC reached similar levels than after 120 min of exercise in the cited study (18) because of the lack of airflow and our higher environmental temperature (36 vs 33°C). Finally, in the trials with airflow at rates similar to Montain and Coyle's (2.55 m·s−1), rehydration lowered core temperature within the 60 min of exercise (W + R vs WIND). All of these findings suggest that without airflow, rehydration has little effect on thermoregulation even during 1 h of exercise in the heat, and, apparently, only the rate of metabolic heat production (similar in CON and REH) determines heat storage.

The finding that the absence of wind offsets the benefits of oral rehydration on heat storage suggests we should be cautious when drawing conclusions based on thermoregulatory studies where airflow is not allowed. For instance, it has been reported that 7 d of heat acclimation does not reduce heat storage during exercise in a 35°C environment (5). In a similar wind-restricted environment it has been found that fluid ingestion to offset dehydration does not affect TREC in comparison to a no fluid ingestion trial (27). The authors of this last study argued that larger dehydration (more than 2.5% body weight loss) should be incurred for fluid ingestion to lower core temperature. In contrast, our data indicate that in the presence of wind, fluid ingestion reduces core temperature and heat storage in exercise bouts lasting 60 min that induce moderate dehydration (i.e., 2.3 ± 0.2%).

In many laboratory studies, the airflow provided is less than what is naturally generated when exercising outdoors. Reviewing the available data, Cheuvront et al. (6) postulate that the increased airflow (to the outdoors levels) would reduce the thermoregulatory strain even in hypohydrated subjects. Saunders et al. (23) have partially confirmed this hypothesis with their observation that at a high airflow (9.3 m·s−1), small differences in dehydration did not affect rectal temperature. It could be speculated that airflow may be superior to rehydration on improving heat dissipation. This is not confirmed in our data, because WIND alone did not significantly reduce TREC below REH (Fig. 1). However, WIND tended to lower TREC and thus it is unknown if application of wind at velocities higher than 2.55 m·s−1 would have significantly reduced TREC. However, it seems unlikely on the basis of data from Saunders et al. (23). They report that the effect of wind cooling on lowering heat storage is almost maximal at a relatively low wind velocity (i.e., 2.75 m·s−1). The typical velocities in running sports range from 2.5 to 5.5 m·s−1, and, thus, the thermal and cardiovascular responses from studies using wind velocities in that range can be validly applied to most sports.

Our results of reduced TREC with W + R in comparison with WIND (Fig. 1) endorse the current thinking (2) that rehydration during exercise in a hot environment benefits heat dissipation, with the important qualification that this is true only when airflow is present. This finding could be relevant to people exercising in an indoors facility especially in the hot season. In some of those indoor facilities, air circulation is substantially less than 2.5 m·s−1, which, together with the humidity induced by sweating, could greatly limit heat dissipation, and hyperthermia might develop. Furthermore, some exercise activities are stationary (i.e., spinning, jogging in a treadmill, stair climbing apparatus, weightlifting) which further limits natural convection flow. On those situations the advice of rehydration should be coupled with assurance of proper ventilation.

The declines in stroke volume (and concomitant heart rate drift) observed during prolonged moderate intensity exercise in the heat have been deemed to be attributable to pooling of blood in the skin veins and reduced venous return (22). During CON and REH (airflow restricted trials), heart rate drifted and stroke volume declined (Table 2). Interestingly, heart rate drift during exercise paralleled the increase in body temperature (higher for CON and REH), yet skin blood flow reached a plateau in all trials at TREC ≈ 38°C. It therefore seems likely that the heart rate drift was more associated with the increases in body temperature rather than induced by blood flow redistribution to the skin. We have previously reported heart rate drift in subjects that was euhydrated but hyperthermic by means of impeding heat dissipation with a plastic jacket (12).

Paradoxically, we observed an increase in whole-body sweat rate in the conditions of higher heat storage (CON and REH). If all the sweat were evaporated, heat storage should have been reduced. Other investigators have reported that increasing air velocity from still air increases whole-body sweat rate at a given level of core temperature (1,19). It is proposed that water accumulation on the skin may inhibit sweat gland activity (19). When sweat rate was plotted against rectal temperature in the restricted wind trials (CON and REH), we did not observe a decline in sweat rate. However, our measurement of sweat rate (nude and dry pre-post body weight) does not distinguish between evaporated and nonevaporative sweat loss. In the Adams et al. study (1), subjects pedaled on a Potter platform balance in which mineral oil film unevaporated sweat was collected. In that study unevaporated sweat loss increased from 1 to 28% when wind was reduced from 3 to 0.2 m·s−1. Likely, most of the increase in sweat rate measured in our experiment when air is restricted corresponded to an inefficient sweating response.

In summary, without airflow, full rehydration does not reduce core temperature relative to that with no rehydration, at least when exercising in the heat with dehydration amounting to 2.3%. Our results indicate that when exercising in a hot environment where evaporative heat loss is the main avenue for heat dissipation (T ambient ≈ T skin) application of wind cannot be neglected. Although wind by itself tended to reduce heat storage (25% below CON) and improve cardiovascular function its effects are greatly enhanced by the combination with rehydration (41% less heat stored than CON).

The authors wish to thank the subjects for their invaluable contribution to the study.

4. Brouwer, E. On simple formulae for calculating the heat expenditure and the quantities of carbohydrate and fat oxidized in metabolism of men and animals, from gaseous exchange (oxygen and carbonic acid output) and urine-N. Acta Physiol. Pharmacol. Neerl. 6:795-802, 1957.

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